Full title: Cancer Associated Fibroblasts are activated in incipient neoplasia to orchestrate tumor promoting inflammation in an NF-B-dependent manner.
Cancer-Associated Fibroblasts Are Activated in Incipient Neoplasia to Orchestrate Tumor-Promoting Inflammation in an NF-kappaB-Dependent Manner.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Otitis media impacts hundreds of mouse middle and inner ear genes.
Age, Specimen part, Treatment
View SamplesObjective: Otitis media is known to alter expression of cytokine and other genes in the mouse middle ear and inner ear. However, whole mouse genome studies of gene expression in otitis media have not previously been undertaken. Ninety-nine percent of mouse genes are shared in the human, so these studies are relevant to the human condition.
Otitis media impacts hundreds of mouse middle and inner ear genes.
Age, Specimen part, Treatment
View SamplesObjective: Otitis media is known to alter expression of cytokine and other genes in the mouse middle ear and inner ear. However, whole mouse genome studies of gene expression in otitis media have not previously been undertaken. Ninety-nine percent of mouse genes are shared in the human, so these studies are relevant to the human condition.
Otitis media impacts hundreds of mouse middle and inner ear genes.
Age, Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Growth factor independence 1b (gfi1b) is important for the maturation of erythroid cells and the regulation of embryonic globin expression.
Specimen part
View SamplesMaintenance of the blood system is dependent on dormant haematopoietic stem cells (HSCs) with long-term self-renewal capacity. Upon injury these cells are induced to proliferate in order to quickly re-establish homeostasis. The signalling molecules promoting the exit of HSCs out of the dormant stage remain largely unknown. Here we show that in response to treatment of mice with interferon-alpha (IFN), HSCs efficiently exit G0 and enter an active cell cycle. HSCs respond to IFN treatment by increased phosphorylation of STAT1 and PKB/Akt, expression of IFN target genes and up-regulation of stem cell antigen-1 (Sca-1). HSCs lacking either the interferon-/ receptor (IFNAR), STAT1 or Sca-1 are insensitive to IFN stimulation, demonstrating that STAT1 and Sca-1 mediate IFN induced HSC proliferation. Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-FU1, HSCs pre-treated (primed) with IFN and thus induced to proliferate are efficiently eliminated by 5-FU exposure in vivo. Conversely, HSCs chronically activated by IFN are functionally compromised and are rapidly out competed by non-activatable IFNAR-/- cells in competitive repopulation assays. In summary, while chronic activation of the IFN pathway in HSCs impairs their function, acute IFN treatment promotes the proliferation of dormant HSCs in vivo. These data may help to clarify the so far unexplained clinical effects of IFN on leukemic cells and raise the possibility for novel applications of type I interferons to target cancer stem cells.
IFNalpha activates dormant haematopoietic stem cells in vivo.
Specimen part, Time
View SamplesThe pathogenic mechanisms of common kidney glomerular diseases, including the vast majority of cases of proteinuria, remain unknown.
Glomerular transcriptome changes associated with lipopolysaccharide-induced proteinuria.
No sample metadata fields
View SamplesAnalysis of HSCs from control and c-myc N-myc deficient long-term hematopoietic stem cells. HSCs lacking both c-myc and N-myc display increased apoptosis rates. Data provide insight into the molecular changes occuring upon complete loss of Myc activity, clarifying the resulting apoptotic mechanism and the role of Myc family proteins in HSCs and commited progenitors.
Hematopoietic stem cell function and survival depend on c-Myc and N-Myc activity.
Age, Specimen part
View SamplesAnalysis of HSCs from control and c-myc N-myc deficient long-term hematopoietic stem cells. HSCs lacking both c-myc and N-myc display increased apoptosis rates. Data provide insight into the molecular changes occuring upon complete loss of Myc activity, clarifying the resulting apoptotic mechanism and the role of Myc family proteins in HSCs.
Hematopoietic stem cell function and survival depend on c-Myc and N-Myc activity.
Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Hematopoietic stem cell function and survival depend on c-Myc and N-Myc activity.
Age, Specimen part
View Samples